From the Department of Medicine, Michigan State University College of Human Medicine, East Lansing, and the College of Health Science, Grand Valley State University, Allendale, Mich.
Recent research has shown that inserting a gene for the protein component
of telomerase into senescent human cells reextends their telomeres to lengths
typical of young cells, and the cells then display all the other identifiable
characteristics of young, healthy cells. This advance not only suggests that
telomeres are the central timing mechanism for cellular aging, but also demonstrates
that such a mechanism can be reset, extending the replicative life span of
such cells and resulting in markers of gene expression typical of "younger"
(ie, early passage) cells without the hallmarks of malignant transformation.
It is now possible to explore the fundamental cellular mechanisms underlying
human aging, clarifying the role played by replicative senescence. By implication,
we may soon be able to determine the extent to which the major causes of death
and disability in aging populations in developed countries—cancer, atherosclerosis,
osteoarthritis, macular degeneration, and Alzheimer dementia—are attributable
to such fundamental mechanisms. If they are amenable to prevention or treatment
by alteration of cellular senescence, the clinical implications have few historic
Fossel M. Telomerase and the Aging Cell: Implications for Human Health. JAMA. 1998;279(21):1732–1735. doi:10.1001/jama.279.21.1732
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